Lung cancer and vehicle exhaust in trucking industry workers

Background

An elevated risk of lung cancer in truck drivers has been attributed to diesel exhaust exposure. Interpretation of these studies specifically implicating diesel exhaust as a carcinogen has been limited because of limited exposure measurements and lack of work records relating job title to exposure-related job duties.

Objectives

We established a large retrospective cohort of trucking company workers to assess the association of lung cancer mortality and measures of vehicle exhaust exposure.

Methods

Work records were obtained for 31,135 male workers employed in the unionized U.S. trucking industry in 1985. We assessed lung cancer mortality through 2000 using the National Death Index, and we used an industrial hygiene review and current exposure measurements to identify jobs associated with current and historical use of diesel-, gas-, and propane-powered vehicles. We indirectly adjusted for cigarette smoking based on an industry survey.

Results

Adjusting for age and a healthy-worker survivor effect, lung cancer hazard ratios were elevated in workers with jobs associated with regular exposure to vehicle exhaust. Mortality risk increased linearly with years of employment and was similar across job categories despite different current and historical patterns of exhaust-related particulate matter from diesel trucks, city and highway traffic, and loading dock operations. Smoking behavior did not explain variations in lung cancer risk.

Conclusions

Trucking industry workers who have had regular exposure to vehicle exhaust from diesel and other types of vehicles on highways, city streets, and loading docks have an elevated risk of lung cancer with increasing years of work.     

Lung Cancer in Chinese Women: Evidence for an Interaction between Tobacco Smoking and Exposure to Inhalants in the Indoor Environment

Background

Epidemiologic data suggest that Chinese women have a high incidence of lung cancer in relation to their smoking prevalence. In addition to active tobacco smoke exposure, other sources of fumes and airborne particles in the indoor environment, such as cooking and burning of incense and mosquito coils, have been considered potential risk factors for lung cancer.

Objectives

We used a case–control study to explore effects of inhalants from combustion sources common in the domestic environment on lung cancer and their modification by active tobacco smoking.

Methods

We analyzed 703 primary lung cancer cases and 1,578 controls. Data on demographic background and relevant exposures were obtained by face-to-face interviews in the hospital.

Results

We observed a positive relationship with daily exposure to incense or mosquito coils and to cooking fumes only among smokers, and no association among lifetime nonsmokers. Interactions between smoking and frequency of cooking, or exposure to incense or mosquito coils were statistically significant and consistent with synergistic effects on lung cancer. The odds ratio (OR) comparing smokers without daily incense or mosquito coil exposure with nonsmokers without daily exposure was 2.80 [95% confidence interval (CI), 1.86–4.21], whereas the OR comparing smokers with daily exposure to the same referent group was 4.61 (95% CI, 3.41–6.24). In contrast, daily exposure to incense or mosquito coils was not associated with lung cancer among nonsmokers (OR = 0.91; 95% CI, 0.72–1.16). We observed the same pattern of associations for smokers without (OR = 2.31; 95% CI, 1.52–3.51) and with (OR = 4.50; 95% CI, 3.21–6.30) daily cooking exposure compared with nonsmokers, with no evidence of an association with daily cooking exposure among nonsmokers.

Conclusion

Our results suggest that active tobacco smoking not only is an important risk factor for development of lung cancer, but also may cause smokers to be more susceptible to the risk-enhancing effects of other inhalants.     

Peer Reviewed: Demographic and Geographic Differences in Exposure to Secondhand Smoke in Missouri Workplaces, 2007-2008

Introduction

African Americans, Hispanics, service and blue-collar workers, and residents of rural areas are among those facing higher rates of workplace secondhand smoke exposure in states without smokefree workplace laws. Consequently, these groups also experience more negative health effects resulting from secondhand smoke exposure. The objective of this study was to examine disparities in workplace secondhand smoke exposure in a state without a comprehensive statewide smokefree workplace law and to use this information in considering a statewide law.

Methods

We developed a logistic multilevel model by using data from a 2007-2008 county-level study to account for individual and county-level differences in workplace secondhand smoke exposure. We included sex, age, race, annual income, education level, smoking status, and rural or urban residence as predictors of workplace secondhand smoke exposure.

Results

Factors significantly associated with increased exposure to workplace secondhand smoke were male sex, lower education levels, lower income, living in a small rural or isolated area, and current smoking. For example, although the overall rate of workplace exposure in Missouri is 11.5%, our model predicts that among young white men with low incomes and limited education living in small rural areas, 40% of nonsmokers and 56% of smokers may be exposed to secondhand smoke at work.

Conclusion

Significant disparities exist in workplace secondhand smoke exposure across Missouri. A statewide smokefree workplace law would protect all citizens from workplace secondhand smoke exposure.     

Vital Signs: Disparities in Nonsmokers’ Exposure to Secondhand Smoke — United States, 1999–2012

Background

Exposure to secondhand smoke (SHS) from burning tobacco causes disease and death in nonsmoking children and adults. No risk-free level of SHS exposure exists.

Methods

National Health and Nutrition Examination Survey (NHANES) data from 1999–2012 were used to examine SHS exposure among the nonsmoking population aged ≥3 years. SHS exposure among nonsmokers was defined as a serum cotinine level (a metabolite of nicotine) of 0.05–10 ng/mL. SHS exposure was assessed overall and by age, sex, race/ethnicity, poverty level, education, and whether the respondent owned or rented their housing.

Results

Prevalence of SHS exposure in nonsmokers declined from 52.5% during 1999–2000 to 25.3% during 2011–2012. During this period, declines were observed for all population subgroups, but disparities exist. During 2011–2012, SHS was highest among: children aged 3–11 years (40.6%), non-Hispanic blacks (46.8%), persons living below the poverty level (43.2%), and persons living in rental housing (36.8%). Among children aged 3–11 years, 67.9% of non-Hispanic blacks were exposed to SHS compared with 37.2% of non-Hispanic whites and 29.9% of Mexican Americans.

Conclusion

Overall, SHS exposure in the United States has been reduced by half since 1999–2000. However, 58 million persons were still exposed to SHS during 2011–2012, and exposure remains higher among children, non-Hispanic blacks, those living in poverty, and those who rent their housing.

Implications for Public Health Practice

Eliminating smoking in indoor spaces fully protects nonsmokers from SHS exposure; separating smokers from nonsmokers, cleaning the air and ventilating buildings cannot completely eliminate exposure. Continued efforts to promote implementation of comprehensive statewide laws prohibiting smoking in workplaces and public places, smoke-free policies in multiunit housing, and voluntary smoke-free home and vehicle rules are critical to protect nonsmokers from this preventable health hazard in the places they live, work, and gather.     

Workplace Exposures and the Risk of Amyotrophic Lateral Sclerosis

Background

Occupation has been suggested to play a role in amyotrophic lateral sclerosis (ALS) etiology, but detailed information on the importance of specific workplace exposures is lacking.

Objectives

Our aim was to assess the relationship between workplace exposures and the risk of ALS and to evaluate potential interactions between these exposures and smoking.

Methods

We conducted a case–control study in New England between 1993 and 1996, comprising 109 cases and 253 controls who completed a structured interview covering occupations and workplace exposures. Unconditional logistic regression models were used to estimate the odds ratios (ORs) and 95% confidence intervals (CIs) for ALS. Analyses were conducted among the entire study population and after stratification by smoking.

Results

We observed a higher risk of ALS for construction workers excluding supervisors (OR = 2.9; 95% CI, 1.2–7.2) and precision metal workers (OR = 3.5; 95% CI, 1.2–10.5). Self-reported exposures to paint strippers; cutting, cooling, or lubricating oils; antifreeze or coolants; mineral or white spirits; and dry cleaning agents each appeared to be associated with a 60–90% higher risk. Specific chemicals related to a > 50% increase in risk of ALS included aliphatic chlorinated hydrocarbons, glycols, glycol ethers, and hexane. Relative risks associated with these workplace exposures and chemicals were greater among nonsmokers and persisted in mutually adjusted models.

Conclusions

Our data suggest that certain occupations and workplace exposures may be associated with increased risk of ALS. These results need to be confirmed in independent populations.     

A Case–Control Study of Lung Cancer Nested in a Cohort of European Asphalt Workers

Background

We conducted a nested case–control study in a cohort of European asphalt workers in which an increase in lung cancer risk has been reported among workers exposed to airborne bitumen fume, although potential bias and confounding were not fully addressed.

Objective

We investigated the contribution of exposure to bitumen, other occupational agents, and tobacco smoking to the risk of lung cancer among asphalt workers.

Methods

Cases were cohort members in Denmark, Finland, France, Germany, the Netherlands, Norway, and Israel who had died of lung cancer between 1980 and the end of follow-up (2002–2005). Controls were individually matched in a 3:1 ratio to cases on year of birth and country. We derived exposure estimates for bitumen fume and condensate, organic vapor, and polycyclic aromatic hydrocarbons, as well as for asbestos, crystalline silica, diesel motor exhaust, and coal tar. Odds ratios (ORs) were calculated for ever-exposure, duration, average exposure, and cumulative exposure after adjusting for tobacco smoking and exposure to coal tar.

Results

A total of 433 cases and 1,253 controls were included in the analysis. The OR was 1.12 [95% confidence interval (CI), 0.84–1.49] for inhalation exposure to bitumen fume and 1.17 (95% CI, 0.88–1.56) for dermal exposure to bitumen condensate. No significant trend was observed between lung cancer risk and duration, average exposure, or cumulative exposure to bitumen fume or condensate.

Conclusions

We found no consistent evidence of an association between indicators of either inhalation or dermal exposure to bitumen and lung cancer risk. A sizable proportion of the excess mortality from lung cancer relative to the general population observed in the earlier cohort phase is likely attributable to high tobacco consumption and possibly to coal tar exposure, whereas other occupational agents do not appear to play an important role.     

Tobacco smoke exposure and altered nasal responses to live attenuated influenza virus

Background

Epidemiologic evidence links tobacco smoke and increased risk for influenza in humans, but the specific host defense pathways involved are unclear.

Objective

We developed a model to examine influenza-induced innate immune responses in humans and test the hypothesis that exposure to cigarette smoke alters nasal inflammatory and antiviral responses to live attenuated influenza virus (LAIV).

Methods

This was an observational cohort study comparing nasal mucosal responses to LAIV among young adult active smokers (n = 17), nonsmokers exposed to secondhand smoke (SHS; n = 20), and unexposed controls (n = 23). Virus RNA and inflammatory factors were measured in nasal lavage fluids (NLF) serially after LAIV inoculation. For key end points, peak and total (area under curve) responses were compared among groups.

Results

Compared with controls, NLF interleukin-6 (IL-6) responses to LAIV (peak and total) were suppressed in smokers. Virus RNA in NLF cells was significantly increased in smokers, as were interferon-inducible protein 10:virus ratios. Responses in SHS-exposed subjects were generally intermediate between controls and smokers. We observed significant associations between urine cotinine and NLF IL-6 responses (negative correlation) or virus RNA in NLF cells (positive correlation) for all subjects combined.

Conclusions

Nasal inoculation with LAIV results in measurable inflammatory and antiviral responses in human volunteers, thus providing a model for investigating environmental effects on influenza infections in humans. Exposure to cigarette smoke was associated with suppression of specific nasal inflammatory and antiviral responses, as well as increased virus quantity, after nasal inoculation with LAIV. These data suggest mechanisms for increased susceptibility to influenza infection among persons exposed to tobacco smoke.     

Factors Associated with Active Smoking,Quitting, and Secondhand Smoke Exposure among Pregnant Women in Greece

Background

Pregnant women are exposed to tobacco smoke through active smoking and contact with secondhand smoke (SHS), and these exposures have a significant impact on public health. We investigated the factors that mediate active smoking, successful quitting, and SHS exposure among pregnant women in Crete, Greece.

Methods

Using a cotinine-validated questionnaire, data were collected on active smoking and exposure to secondhand smoke from 1291 women who had successfully completed the first contact questionnaire of the prospective mother-child cohort (Rhea) in Crete during the 12th week of pregnancy.

Results

Active smoking at some time during pregnancy was reported by 36% of respondents, and 17% were current smokers at week 12 of gestation. Those less likely to quit smoking during pregnancy were those married to a smoker (OR, 1.76; P = 0.008), those who were multiparous (1.72; P = 0.011), and those with young husbands. Of the 832 (64%) nonsmokers, almost all (94%, n = 780) were exposed to SHS, with the majority exposed at home (72%) or in a public place (64%). Less educated women and younger women were exposed more often than their better educated and older peers (P < 0.001). Adjusting for potential confounders, parental level of education, age, and ethnicity were the main mediators of exposure to SHS during pregnancy.

Conclusions

Active smoking and exposure to SHS are very prevalent among pregnant women in Greece. The above findings indicate the need for support of population-based educational interventions aimed at smoking cessation in both parents, as well as of the importance of establishing smoke-free environments in both private and public places.Key words: smoking, cessation, pregnancy, fetal health, passive smoking, SHS     

Sources of Mercury Exposure for U.S. Seafood Consumers: Implications for Policy

Background

Recent policies attempting to reduce adverse effects of methylmercury exposure from fish consumption in the United States have targeted reductions in anthropogenic emissions from U.S. sources.

Objectives

To analyze the prospects for future North American and international emissions controls, we assessed the potential contributions of anthropogenic, historical, and natural mercury to exposure trajectories in the U.S. population over a 40-year time horizon.

Methods

We used models that simulate global atmospheric chemistry (GEOS-Chem); the fate, transport, and bioaccumulation of mercury in four types of freshwater ecosystems; and mercury cycling among different ocean basins. We considered effects on mercury exposures in the U.S. population based on dietary survey information and consumption data from the sale of commercial market fish.

Results

Although North American emissions controls may reduce mercury exposure by up to 50% for certain highly exposed groups such as indigenous peoples in the Northeast, the potential effects of emissions controls on populations consuming marine fish from the commercial market are less certain because of limited measurements.

Conclusions

Despite uncertainties in the exposure pathway, results indicate that a combination of North American and international emissions controls with adaptation strategies is necessary to manage methylmercury risks across various demographic groups in the United States.     

Exposure of the U.S. Population to Acrylamide in the National Health and Nutrition Examination Survey 2003–2004

Background

The lifelong exposure of the population to acrylamide has raised concerns about the possible health effects of the chemical. Data on the extent of exposure to acrylamide and its primary metabolite, glycidamide, are needed to aid in the assessment of potential health effects.

Objectives

The aim of this study was to assess human exposure to acrylamide and glycidamide in the general U.S. population through the measurement of hemoglobin adducts of acrylamide (HbAA) and glycidamide (HbGA).

Methods

HbAA and HbGA were measured in 7,166 subjects from the National Health and Nutrition Examination Survey. Stratified HbAA and HbGA data were reported by sex, age groups, race/ethnicity (Mexican American, non-Hispanic black, non-Hispanic white), and smoking status based on serum cotinine levels. Covariate-adjusted geometric means for each demographic group were calculated using multiple regression analysis.

Results

HbAA and HbGA levels ranged from 3 to 910 and from 4 to 756 pmol/g hemoglobin, respectively, with smokers having the highest levels overall. Tobacco smoke exposure in nonsmokers had a small but significant effect on HbAA and HbGA levels. Adjusted geometric mean levels for children 3–11 years of age were higher than for adults ≥ 60 years of age [mean (95% confidence interval): HbAA, 54.5 (49.1–51.5) and HbGA, 73.9 (71.3–76.6) vs. HbAA, 46.2 (44.3–48.2) and HbGA, 41.8 (38.7–45.2)]. Levels were highest in Mexican Americans [HbAA: 54.8 (51.9–57.8), HbGA: 57.9 (53.7–62.5)], whereas non-Hispanic blacks had the lowest HbGA levels [43.5 (41.1–45.9)].

Conclusions

U.S. population levels of acrylamide and glycidamide adducts are described. The high variability among individuals but modest differences between population subgroups suggest that sex, age, and race/ethnicity do not strongly affect acrylamide exposure. Adduct concentration data can be used to estimate relative exposure and to validate intake estimates.     

Glutathione S-Transferase Polymorphisms,Passive Smoking,Obesity, and Heart Rate Variability in Nonsmokers

Background

Disturbances of heart rate variability (HRV) may represent one pathway by which second-hand smoke (SHS) and air pollutants affect cardiovascular morbidity and mortality. The mechanisms are poorly understood.

Objectives

We investigated the hypothesis that oxidative stress alters cardiac autonomic control. We studied the association of polymorphisms in oxidant-scavenging glutathione S-transferase (GST) genes and their interactions with SHS and obesity with HRV.

Methods

A total of 1,133 nonsmokers > 50 years of age from a population-based Swiss cohort underwent ambulatory 24-hr electrocardiogram monitoring and reported on lifestyle and medical history. We genotyped GSTM1 and GSTT1 gene deletions and a GSTP1 (Ile105Val) single nucleotide polymorphism and analyzed genotype–HRV associations by multiple linear regressions.

Results

Homozygous GSTT1 null genotypes exhibited an average 10% decrease in total power (TP) and low-frequency-domain HRV parameters. All three polymorphisms modified the cross-sectional associations of HRV with SHS and obesity. Homozygous GSTM1 null genotypes with > 2 hr/day of SHS exposure exhibited a 26% lower TP [95% confidence interval (CI), 11 to 39%], versus a reduction of −5% (95% CI, −22 to 17%) in subjects with the gene and the same SHS exposure compared with GSTM1 carriers without SHS exposure. Similarly, obese GSTM1 null genotypes had, on average, a 22% (95% CI, 12 to 31%) lower TP, whereas with the gene present obesity was associated with only a 3% decline (95% CI, −15% to 10%) compared with nonobese GSTM1 carriers.

Conclusions

GST deficiency is associated with significant HRV alterations in the general population. Its interaction with SHS and obesity in reducing HRV is consistent with an impact of oxidative stress on the autonomous nervous system.     

Association between traffic-related black carbon exposure and lung function among urban women

Background

Although a number of studies have documented the relationship between lung function and traffic-related pollution among children, few have focused on adult lung function or examined community-based populations.

Objective

We examined the relationship between black carbon (BC), a surrogate of traffic-related particles, and lung function among women in the Maternal–Infant Smoking Study of East Boston, an urban cohort in Boston, Massachusetts.

Methods

We estimated local BC levels using a validated spatiotemporal land-use regression model, derived using ambient and indoor monitor data. We examined associations between percent predicted pulmonary function and predicted BC using linear regression, adjusting for sociodemographics (individual and neighborhood levels), smoking status, occupational exposure, type of cooking fuel, and a diagnosis of asthma or chronic bronchitis.

Results

The sample of 272 women 18–42 years of age included 57% who self-identified as Hispanic versus 43% white, and 18% who were current smokers. Mean ± SD predicted annual BC exposure level was 0.62 ± 0.2 μg/m³. In adjusted analysis, BC (per interquartile range increase) was associated with a 1.1% decrease [95% confidence interval (CI), −2.5% to 0.3%] in forced expiratory volume in 1 sec, a 0.6% decrease (95% CI, −1.9% to 0.6%) in forced vital capacity, and a 3.0% decrease (95% CI, −5.8% to −0.2%) in forced mid-expiratory flow rate. We noted differential effects by smoking status in that former smokers were most affected by BC exposure, whereas current smokers were not affected.

Conclusion

In this cohort, exposure to traffic-related BC, a component of particulate matter, independently predicted decreased lung function in urban women, when adjusting for tobacco smoke, asthma diagnosis, and socioeconomic status.     

Biological Monitoring for Depleted Uranium Exposure in U.S. Veterans

Background

As part of an ongoing medical surveillance program for U.S. veterans exposed to depleted uranium (DU), biological monitoring of urine uranium (U) concentrations is offered to any veteran of the Gulf War and those serving in more recent conflicts (post-Gulf War veterans).

Objectives

Since a previous report of surveillance findings in 2004, an improved methodology for determination of the isotopic ratio of U in urine (²³⁵U:²³⁸U) has been developed and allows for more definitive evaluation of DU exposure. This report updates previous findings.

Methods

Veterans provide a 24-hr urine specimen and complete a DU exposure questionnaire. Specimens are sent to the Baltimore Veterans Affairs Medical Center for processing. Uranium concentration and isotopic ratio are measured using ICP-MS at the Armed Forces Institute of Pathology.

Results

Between January 2003 and June 2008, we received 1,769 urine specimens for U analysis. The mean urine U measure was 0.009 μg U/g creatinine. Mean urine U concentrations for Gulf War and post-Gulf War veterans were 0.008 and 0.009 μg U/g creatinine, respectively. Only 3 of the 1,700 (0.01%) specimens for which we completed isotopic determination showed evidence of DU. Exposure histories confirmed that these three individuals had been involved in “friendly fire” incidents involving DU munitions or armored vehicles.

Conclusions

No urine U measure with a “depleted” isotopic signature has been detected in U.S. veterans without a history of retained DU embedded fragments from previous injury. These findings suggest that future DU-related health harm is unlikely in veterans without DU fragments.     

Model Development and Validation of Personal Exposure to Volatile Organic Compound Concentrations

Background

Direct measurement of exposure to volatile organic compounds (VOCs) via personal monitoring is the most accurate exposure assessment method available. However, its wide-scale application to evaluating exposures at the population level is prohibitive in terms of both cost and time. Consequently, indirect measurements via a combination of microenvironment concentrations and personal activity diaries represent a potentially useful alternative.

Objective

The aim of this study was to optimize a model of personal exposures (PEs) based on microenvironment concentrations and time/activity diaries and to compare modeled with measured exposures in an independent data set.

Materials

VOC PEs and a range of microenvironment concentrations were collected with active samplers and sorbent tubes. Data were supplemented with information collected through questionnaires. Seven models were tested to predict PE to VOCs in 75% (n = 370) of the measured PE data set, whereas the other 25% (n = 120) was used for validation purposes.

Results

The best model able to predict PE with independence of measurements was based upon stratified microenvironment concentrations, lifestyle factors, and individual-level activities. The proposed model accounts for 40–85% of the variance for individual VOCs and was validated for almost all VOCs, showing normalized mean bias and mean fractional bias below 25% and predicting 60% of the values within a factor of 2.

Conclusions

The models proposed identify the most important non-weather-related variables for VOC exposures; highlight the effect of personal activities, use of solvents, and exposure to environmental tobacco smoke on PE levels; and may assist in the development of specific models for other locations.     

Inhalative Exposure to Vanadium Pentoxide Causes DNA Damage in Workers: Results of a Multiple End Point Study

Background

Inhalative exposure to vanadium pentoxide (V₂O₅) causes lung cancer in rodents.

Objective

The aim of the study was to investigate the impact of V₂O₅ on DNA stability in workers from a V₂O₅ factory.

Methods

We determined DNA strand breaks in leukocytes of 52 workers and controls using the alkaline comet assay. We also investigated different parameters of chromosomal instability in lymphocytes of 23 workers and 24 controls using the cytokinesis-block micronucleus (MN) cytome method.

Results

Seven of eight biomarkers were increased in blood cells of the workers, and vanadium plasma concentrations in plasma were 7-fold higher than in the controls (0.31 μg/L). We observed no difference in DNA migration under standard conditions, but we found increased tail lengths due to formation of oxidized purines (7%) and pyrimidines (30%) with lesion-specific enzymes (formamidopyrimidine glycosylase and endonuclease III) in the workers. Bleomycin-induced DNA migration was higher in the exposed group (25%), whereas the repair of bleomycin-induced lesions was reduced. Workers had a 2.5-fold higher MN frequency, and nucleoplasmic bridges (NPBs) and nuclear buds (Nbuds) were increased 7-fold and 3-fold, respectively. Also, apoptosis and necrosis rates were higher, but only the latter parameter reached statistical significance.

Conclusions

V₂O₅ causes oxidation of DNA bases, affects DNA repair, and induces formation of MNs, NPBs, and Nbuds in blood cells, suggesting that the workers are at increased risk for cancer and other diseases that are related to DNA instability.     

Neurobehavioral Deficits and Increased Blood Pressure in School-Age Children Prenatally Exposed to Pesticides

Background

The long-term neurotoxicity risks caused by prenatal exposures to pesticides are unclear, but a previous pilot study of Ecuadorian school children suggested that blood pressure and visuospatial processing may be vulnerable.

Objectives

In northern Ecuador, where floriculture is intensive and relies on female employment, we carried out an intensive cross-sectional study to assess children’s neurobehavioral functions at 6–8 years of age.

Methods

We examined all 87 children attending two grades in the local public school with an expanded battery of neurobehavioral tests. Information on pesticide exposure during the index pregnancy was obtained from maternal interview. The children’s current pesticide exposure was assessed from the urinary excretion of organophosphate metabolites and erythrocyte acetylcholine esterase activity.

Results

Of 84 eligible participants, 35 were exposed to pesticides during pregnancy via maternal occupational exposure, and 23 had indirect exposure from paternal work. Twenty-two children had detectable current exposure irrespective of their prenatal exposure status. Only children with prenatal exposure from maternal greenhouse work showed consistent deficits after covariate adjustment, which included stunting and socioeconomic variables. Exposure-related deficits were the strongest for motor speed (Finger Tapping Task), motor coordination (Santa Ana Form Board), visuospatial performance (Stanford-Binet Copying Test), and visual memory (Stanford-Binet Copying Recall Test). These associations corresponded to a developmental delay of 1.5–2 years. Prenatal pesticide exposure was also significantly associated with an average increase of 3.6 mmHg in systolic blood pressure and a slight decrease in body mass index of 1.1 kg/m². Inclusion of the pilot data strengthened these results.

Conclusions

These findings support the notion that prenatal exposure to pesticides—at levels not producing adverse health outcomes in the mother—can cause lasting adverse effects on brain development in children. Pesticide exposure therefore may contribute to a “silent pandemic” of developmental neurotoxicity.     

Secondhand smoke exposure among women and children: evidence from 31 countries

Objectives. We sought to describe the range of exposure to secondhand smoke (SHS) among women and children living with smokers around the world and generate locally relevant data to motivate the development of tobacco control policies and interventions in developing countries.Methods. In 2006, we conducted a cross-sectional exposure survey to measure air nicotine concentrations in households and hair nicotine concentrations among nonsmoking women and children in convenience samples of 40 households in 31 countries.Results. Median air nicotine concentration was 17 times higher in households with smokers (0.18 μg/m³) compared with households without smokers (0.01 μg/m³). Air nicotine and hair nicotine concentrations in women and children increased with the number of smokers in the household. The dose–response relationship was steeper among children. Air nicotine concentrations increased an estimated 12.9 times (95% confidence interval=9.4, 17.6) in households allowing smoking inside compared with those prohibiting smoking inside.Conclusions. Our results indicate that women and children living with smokers are at increased risk of premature death and disease from exposure to SHS. Interventions to protect women and children from household SHS need to be strengthened.Extensive research shows that secondhand smoke (SHS) exposure places adults and children at increased risk for premature death, diverse illnesses, and other adverse effects, such as reduced lung-function growth in children.1 Worldwide, over 40% of men smoke tobacco, compared with only about 12% of women.2 This global profile implies that women and children constitute the bulk of the population exposed to SHS. The World Health Organization (WHO) conducted the Global Youth Tobacco Survey between 1999 and 2005 and found that approximately 44% of youths were exposed to tobacco smoke at home and that 47% had at least 1 parent who smoked.3 There is insufficient information, however, regarding levels of SHS in households and the range of exposures among women and children throughout the world. Questionnaires have been the most commonly used tool to assess the prevalence and intensity of SHS exposure at home.3^–5 Although questionnaires can confirm that SHS exposure is taking place, they are not highly informative as to the specific level of exposure because of inherent limitations of the data collected.1For our study, we sought to quantify the levels of SHS exposure among women and children living with smokers in diverse climates and cultures. Measuring air nicotine and hair nicotine concentrations are validated methods of quantifying airborne levels of SHS and the uptake of SHS in the body, respectively.6^,7 We carried out a multicountry study measuring nicotine concentrations in the air of households with and without smokers and in the hair of women and children living in these households. Survey data were also collected to evaluate smoking behaviors and smoking policies in the households and around the children, as well as perceptions and attitudes about SHS.     

Did Smokefree Legislation in England Reduce Exposure to Secondhand Smoke among Nonsmoking Adults? Cotinine Analysis from the Health Survey for England

Background

On 1 July 2007, smokefree legislation was implemented in England, which made virtually all enclosed public places and workplaces smokefree.

Objectives

We examined trends in and predictors of secondhand smoke exposure among nonsmoking adults to determine whether exposure changed after the introduction of smokefree legislation and whether these changes varied by socioeconomic status (SES) and by household smoking status.

Methods

We analyzed salivary cotinine data from the Health Survey for England that were collected in 7 of 11 annual surveys undertaken between 1998 and 2008. We conducted multivariate regression analyses to examine secondhand smoke exposure as measured by the proportion of nonsmokers with undetectable levels of cotinine and by geometric mean cotinine.

Results

Secondhand smoke exposure was higher among those exposed at home and among lower-SES groups. Exposure declined markedly from 1998 to 2008 (the proportion of participants with undetectable cotinine was 2.9 times higher in the last 6 months of 2008 compared with the first 6 months of 1998 and geometric mean cotinine declined by 80%). We observed a significant fall in exposure after legislation was introduced—the odds of having undetectable cotinine were 1.5 times higher [95% confidence interval (CI): 1.3, 1.8] and geometric mean cotinine fell by 27% (95% CI: 17%, 36%) after adjusting for the prelegislative trend and potential confounders. Significant reductions were not, however, seen in those living in lower-social class households or homes where smoking occurs inside on most days.

Conclusions

We found that the impact of England’s smokefree legislation on secondhand smoke exposure was above and beyond the underlying long-term decline in secondhand smoke exposure and demonstrates the positive effect of the legislation. Nevertheless, some population subgroups appear not to have benefitted significantly from the legislation. This finding suggests that these groups should receive more support to reduce their exposure.     

Secondhand smoke exposure in young people and parental rules against smoking at home and in the car

Objectives

Secondhand smoke (SHS) exposure is an important cause of morbidity in children. We assessed the impact of family rules about smoking in the home and car on SHS exposure prevalence in students in grades six to 12.

Methods

We studied never-smoking young people (n=1,698) in the random sample cross-sectional South Carolina Youth Tobacco Survey, a 2006 survey of middle and high school students in South Carolina.

Results

Overall, 40% of the students reported SHS exposure in either the home or car in the past week; among these, 85% reported exposure in cars. Subsequent analyses focused on students who lived with a smoker (n=602). Compared with those whose families prohibited smoking in the home or car, SHS exposure prevalence was 30% (p<0.0001) higher for households with smoke-free rules for only one place (home or car) and 36% (p<0.0001) higher for households with no rules. Compared with students from households with strict rules, SHS exposure prevalence was 48% greater (p<0.0001) among those with only partial rules against smoking in the home or car, and 55% (p<0.0001) greater among those from households with no rules. Similarly, compared with students with strict family rules for home and car that were adhered to, SHS exposure prevalence was significantly higher (p<0.0001) among students when only one or no rules were followed.

Conclusions

Young people from families that made and enforced strong rules against smoking in homes and cars were much less likely to report SHS exposure. Parents would be wise to endorse and enforce strong smoke-free policies for both homes and cars.Secondhand smoke (SHS) exposure is associated with many adverse health effects on children including sudden infant death syndrome, respiratory infections, asthma, and otitis media.¹ The established negative effects of SHS on child health have led the American Academy of Pediatrics^2,3 and the American Medical Association⁴ to urge pediatricians and physicians in other medical specialties to assist parents in protecting their children from tobacco smoke.The two places where children may be at greatest risk of SHS exposure are family homes and cars. One way that parents can protect their children from SHS exposure is to make rules prohibiting smoking in these places. Thus far, studies of rulemaking have tended to focus on SHS exposure in homes,^5–14 with results suggesting that establishing strong smoke-free rules in homes is a promising strategy to reduce children''s household exposure to SHS.Given the concentrated pollution levels found within the small enclosed area of a car,¹⁵ rules to protect children against SHS exposure in cars may be important. The study of children''s exposure to SHS in cars is a timely topic given that some states, such as Arkansas, California, Louisiana, and Maine, have enacted legislation against smoking in the car when children are present. However, cars have received relatively scant attention from researchers as a source of SHS exposure. Little is known about the prevalence of SHS exposure in cars, let alone whether rules prohibiting smoking in cars are beneficial in reducing SHS exposure in young people. Previous studies to report on the relationship between rules against smoking in the car and SHS exposure generated promising findings, indicating that smoking bans in cars were associated with a sevenfold decrease in children''s SHS exposure¹³ and significant reductions in salivary cotinine levels, a biomarker of SHS exposure.¹⁶Family rules concerning smoke-free homes and cars can be effective toward establishing a smoke-free environment only to the extent that such rules are enforced. Few studies have considered the impact of both rulemaking and rule enforcement on SHS exposure. The only previous report to explore how completeness of smoke-free rules affects SHS exposure was not a study of child SHS exposure.⁵ To address these current gaps in the evidence, we assessed the influence on children''s SHS exposure of family rulemaking and rule enforcement related to smoking in the home and in the car.     

Respiratory Cancer and Inhaled Inorganic Arsenic in Copper Smelters Workers: A Linear Relationship with Cumulative Exposure that Increases with Concentration

Background

Inhalation of high levels of airborne inorganic arsenic is a recognized cause of respiratory cancer. Although multiple epidemiologic studies have demonstrated this association, there have been few analyses of the mathematical relationship between cumulative arsenic exposure and risk of respiratory cancer, and no assessment as to whether and how arsenic concentration may modify this association.

Objectives

The objective is an evaluation of the shape of the relationship between respiratory cancer mortality and cumulative inhaled arsenic exposure among copper smelter workers, and the modification of that relationship by arsenic concentration.

Methods

We used Poisson regression methods to analyze data from a cohort of arsenic-exposed copper smelter workers under a linear-exponential model for the excess relative risk.

Results

Within categories of arsenic concentration, the association between respiratory cancer and cumulative arsenic exposure was consistent with linearity. The slope of the linear relationship with cumulative exposure increased with increasing arsenic concentration category.

Conclusions

Our results suggested a direct concentration effect from inhaled inorganic arsenic, whereby the excess relative risk for a fixed cumulative exposure was greater when delivered at a higher concentration and shorter duration than when delivered at a lower concentration and longer duration.